Acne in pregnancy

Chapter 9
Acne in pregnancy

Babies are precious, so the management of acne before an intended pregnancy and during pregnancy is limited in several ways. Obviously, the first concern is the protection of the unborn child. This means that there is much greater need for care in the selection of therapy than usual.

The subjects that most mothers-to-be worry about are the drugs and other chemicals in the environment. Some of the threats posed by medications are real, they are proven, and they are based on science, as is the case with isotretinoin (better known as Accutane, Roaccutane, and about 10 other generic names around the world). Other reported risks are suspected but unproven, or based on less than perfect science, such as the suggestion that topical salicylic acid be avoided (discussed further in this chapter). And then there is the broad field of untested drugs and “supplements.”

Because of the threat of litigation in the event of a less than perfect baby being born, universal caution is advised and risk avoidance has become the general self-protective rule for all cautious advisors and prescribers. The legal situation is made even more unsatisfactory for both physicians and patients by the lack of available safety data. This is, of course, because it is obviously impossible to conduct appropriately blinded medication trials in the “population at risk.” You will never hear “We have this new drug, Mrs. Jones, and we’d like to have you try it during your pregnancy to see what will happen.” That means that information on virtually all drugs is incomplete, and any use of any drug prior to conception and during pregnancy is considered on the basis of risk versus benefit. Every case is different.

Despite this problem, safe and rational management of acne prior to and during pregnancy is available. That means first of all that one should step back and take a cautious look from a distance. First, we need to consider whether the problem being treated is preventable. If so, then prevention should be the prime consideration, a subject covered in Section 8.1. Then we need to look at the active therapies available, and we need to know what is likely to happen without the medication that is being considered. Then the question of active therapy should be considered by carefully searching first for the safest approach possible. This means avoiding any topical or systemic medications that might cast a shadow across the unborn child’s future.

9.1 Epidemiology

The incidence of acne in pregnancy is really not relevant in a population that suffers an 85–90% lifetime risk of this disorder. Epidemiology studies populations, not single pregnancies. Furthermore, epidemiology is of no use in predicting or explaining the appearance of significant acne in a single pregnancy. The practical approach says simply, “A problem will either happen, or it will not—it is 50:50.” The difficulty is that acne may arrive totally unexpectedly and may be totally unrelated to the mother’s prior clear-skinned, nonpregnant state. The only thing that is predictable is that acne’s appearance in pregnancy is unpredictable. Preexisting acne can disappear with the same unpredictability.

9.2 Pathogenesis

To define the strategy for managing acne in pregnancy, one first needs an understanding of three facets of the disease:

The primary pathological processes that lead to the microcomedo that plugs the pore
The inflammatory reactions downstream from the primary disease process
The various treatments (including prevention) that are generally recognized as safe (and are as effective as possible).

The first two points are covered in previous chapters (Chapter 3 and Section 8.1), and this chapter will deal with prevention and therapy of acne before, during, and after pregnancy.

For many years, acne in pregnancy had been thought to be caused by the pregnancy itself. It was known that there were increases in the amount of normal male hormones (androgens and some relatives that can turn into androgens) made by the ovaries and by the adrenal (stress) glands. We thought these normal hormones were supplemented by more adrenal androgens that were caused by the stresses of pregnancy.

Indeed, this was considered an exaggerated form of the changes that Lucky demonstrated in showing the relationship of acne flares to the hormones produced during the luteal phase of the menstrual cycle [1] The luteal phase is the time after midcycle, so it is just after ovulation and before the period arrives, when the ovary produces more progesterone than at any other time, getting the uterus ready for a baby. If there is no baby, the progesterone level drops, the lining of the uterus is shed as period flow, and the “period acne” clears.

But, if there IS a pregnancy, the spot on the ovary that produced the egg goes on to form a yellow bump on the ovary called the corpus luteum (Latin for yellow body). In the initial stages of pregnancy, this collection of cells produces substantial amounts of progesterone (30 mg per day) and 5α-pregnanedione [2, 3]. Both these chemicals can turn into androgen, especially dihydrotestosterone (DHT), right in the folliculopilosebaceous unit (FPSU) itself. And DHT is the major cause of acne.

This ovarian influence normally fades beginning at six weeks of gestation, and the mother’s placenta takes over as a prime source of progesterone, producing up to 300 mg per day of progesterone until delivery, and twice that or more in twins or multiple pregnancies [4]. The placenta also produces several other steroids, many of which are androgen precursors. This hormone output, which is supposed to go to the baby, is normally kept on the baby’s side of the placenta, but some does reach the mother’s circulation, mainly to maintain the link between the uterus and the placenta in good shape, and this may cause acne in some pregnancies. More research on placental hormones needs to be done, particularly in view of the fact that early studies were done on term (nine-month or post-delivery) placentas. These are basically aging placentas whose hormonal metabolic activities are slowing down. Ultimately they are failing or have failed as a fetal support system, and it is this failure that brings on labor contractions. But obtaining fresh healthy first-term and midterm placentas to study is understandably almost impossible.

The other possible source of hormones that turn into DHT in a small percentage of pregnancies may be from persistent corpus luteum progesterone production, beyond that described here. In other primates (like monkeys), this can be caused by the corpus luteum being exposed to an early rise in pregnancy-induced chorionic gonadotropin from the placenta [5]. The problem here is that what we don’t know about the hormones produced by the human placenta would likely fill several books. This is understandable given the difficulties involved in studying such tissue.

The stress of pregnancy itself can be expected to produce both adrenal androgens (more DHT precursors) [6, 7] and more corticotropin-releasing hormone (CRH) [8]. Both of these tend to promote acne. CRH turns on the steroid hormones from the adrenals through its messenger, ACTH, but it also seems to have a direct effect on the FPSU as well. The CRH story is new, so you will need to look at Section 1.41 (and Figure 1.40) for further details.

In addition to starting the comedo/blackhead pore-plugging process, the androgens attaching to the androgen receptors on the FPSU also stimulate an overproduction of sebum at the same time. There are steps in between that make for a very complicated set of reactions all in a row, all leading to the plugged pore. Remember that the acne process is ultimately regulated by the androgen (male) receptor. The problem in managing acne in pregnancy is that there is no medicine considered safe during pregnancy that we can use to actively block this receptor. It would be great to keep the receptor closed to prevent it from catching any androgens, but this is not practical. The only easily available, safe, and reasonably effective approach is to reduce the level of androgen receptor activity by reducing the levels of both insulin and IGF-1. That will allow the androgen receptor to return to its normal adult repressed (unreceptive and resting “closed”) state, allowing the androgen-driven system to cool down, and the resulting acne to fade.

In summary, there is no available, acceptable, safe, and specific medication that can be used during pregnancy to block the effect of these important but acne-causing hormones, and of course investigation and development of such molecular intervention are next to impossible because of the risks to the study population (mom and baby).

9.3 Team up with Mother Nature

Fortunately, there is a simple, physiological, totally time-tested, and indeed healthy approach available. All that is needed is total dairy avoidance, preferably combined with a diet with serious restriction of high-glycemic-load (HGL: sugary and glucose-producing) foods. It is a big step for those of us raised on a Western diet, but simple science suggests that moving to such a diet is the most logical of all possible steps in the right direction. If you cannot do without some sort of fluid “milk,” then it is time to try dairy substitutes. Look around for those made with soy, almonds, rice, coconut, or hemp, but take care to select only those that are “unsweetened” to lower the glycemic load. Save the chocolate and the French vanilla for occasional special treats only.

Then there is another simple “no-brainer.” Stop smoking. Smoking as a possible cause of acne has been recognized anecdotally for years, but there is some new science to think about. Smoking is now linked with comedonal post-adolescent acne (so-called adult acne) as well as acne inversa/hidradenitis suppurativa (AI/HS) [9, 10]. In addition to discontinuing smoking for its deleterious cardiac and pulmonary effects on the mother, it should be eliminated in all patients with acne, and particularly in pregnancy, because of fetal concerns. The same is true in AI/HS.

9.4 Targeting therapy

There are three traditional targets of acne therapy. These are the physical plugs that require prevention and comedolytics, the organisms and debris in the duct that need various drugs for their control and elimination, and the inflammation that requires cooling. All three targets must be addressed in organizing a logical attack on acne. The solutions to the problem are limited by the “delicate condition” of pregnancy.

9.4.1 Clinical manifestations

There is really no difference in the presentation of acne between pregnant and nonpregnant women. Acne may suddenly appear in its most aggressive form for the first time in previously clear skin, or previously active acne may simply vanish in the glow of a new pregnancy. Similarly, it may disappear after delivery or it may recur in the postpartum period. Curiously, it may occur in some pregnancies but not others, despite identical parents. Every case, like every woman, is unique.

9.4.2 Pathology

There are no pathologic findings that are specific to acne in pregnancy that differentiate it from the acnes (vulgaris, rosacea, or inversa) of nonpregnancy.

9.4.3 Diagnostic evaluation

All true acne at any time is driven by hormones. The additional complexity of pregnancy hormones requires a careful evaluation of all sources of acnegenic hormones, both steroids and polypeptides. An extensive historical review of dietary habits is essential. Expensive laboratory investigation should be reserved for those whose acne is unusual. By that I mean it is sudden in onset, is accompanied by signs of androgen excess, is highly inflammatory, fails to respond to the exclusion of exogenous acnegens (including those supplied or induced by dairy and HGL diets), or is otherwise inexplicable. Drug history is especially important, as the offending substance (such as anabolic steroids used by bodybuilders—even some women) may be illicit and may be carefully hidden away behind maternal guilt. Diplomatic probing for a history of bodybuilding, use of whey- and casein-containing protein powder, and use of other bodybuilding supplements can lead gently to the question of anabolic steroid use.

In searching for acnegens, both the physician and the pregnant patient must realize that the elevations in insulin and IGF-1 that lead to de-repression (opening) of the androgen receptor are triggered by fluid milk (whether skim or whole) [11] and by ingestion of the whey and casein found in protein supplements [12], in addition to all the more easily recognized dairy products and the sugars and their easily digested carbohydrates. The androgen receptors, sensitized by dietary polypeptide hormones, open up and wait for the steroid hormones from both the normal nonpregnant sources (ovaries, adrenals and the intracrine system) and the overflow from the daily production of 300 mg of progesterone plus related steroids from the placenta [4]. Detecting anabolic steroids added from the outside is more important here than in Olympic athletes.

9.4.4 Overview and general approach to treatment

In the vulnerable mother and unborn baby, prevention of the disorder should take logical priority, so the first order of business is to define the steps that can be directed at the primary lesion, the comedo. Tactics must be designed and implemented to prevent the formation of new plugs, stop the progression of plugs that have gotten underway, and empty out the established plugs.

The single, and the healthiest, change (for both mother and baby) available to all is to adopt a zero-dairy and low-glycemic-load (LGL) diet. Dairy products, refined sugar, and refined wheat-based products were simply not part of the human diet until relatively recently, and the amounts of these we presently consume are immense compared to what our grandparents grew up with. For example, in the United States, the volume of cheese consumed per person is five times now what it was 35 years ago. In Japan, the amount of dairy product consumed per person per year went up from 5.5 lbs. to an astounding 117.4 lbs. between 1950 and 1975 [13]. Our bodies were simply not designed to handle these changes.

Fortunately, there is an answer to all this, the so-called Paleolithic diet. There is no diet available that more closely conforms to the diet that our bodies were designed for than this diet. For instance, consider lactose intolerance. Although some of the human population experienced the mutation of a gene about 15,000 years ago that now permits lactose in our diets, most of the human race has simply not evolved to handle the lactose in milk. Dairy products also normally contain significant levels of reproductive hormones, numerous polypeptide hormones, and growth factors. Refined wheat products fill the shelves of our grocery and “convenience” stores. Sugars are presented to us in seductive, attractive, and even addictive modern foods. These come to us courtesy of modern farming, selective breeding, and food production and marketing techniques. The milkman, the bread man, and the snack, soda, and soft drink sales force did not visit the caveman and his pregnant mate, nor should they visit the modern pregnant woman.

The Aché tribe studied by Cordain considers the practice of drinking the milk of another species “abhorrent” [14]. It strikes me as very curious that we think that they are primitive. It is disconcerting at best to realize that we know more about the hormonal exposure of Olympic athletes, baseball players, Tour de France winners, Greek weightlifters, and racehorses in Pennsylvania than we do about the hormones in the dairy products we feed to our children, grandchildren, and expectant mothers.

Drinking milk and eating dairy-based products are, quite simply, not a challenge for which evolution has prepared us. No other species knowingly exposes its pregnant females, let alone their offspring in utero, to the hormones and growth factors in dairy products. To resort to instructive hyperbole, we all need to be acutely aware that cows do not drink milk after weaning or while pregnant, and they most certainly are not fed milk from pregnant humans. Likewise, adult humans generally recognize that they should respect the weaning process as far as their own mothers are concerned.